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Treatment is symptomatic No therapy has been shown to slow disease progression, but trials of several putative neuroprotective agents are in progress, as are various trials of gene therapy
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Drug treatment is not required early in the course of parkinsonism, but the nature of the disorder and the availability of medical treatment for use when necessary should be discussed with the patient 1 Amantadine Patients with mild symptoms but no disability may be helped by amantadine This drug improves all of the clinical features of parkinsonism, but its mode of action is unclear Side effects include restlessness, confusion, depression, skin rashes, edema, nausea, constipation, anorexia, postural hypotension, and disturbances of cardiac rhythm However, these are relatively uncommon with the usual dose (100 mg twice daily) 2 Anticholinergic drugs Anticholinergics are more helpful in alleviating tremor and rigidity than bradykinesia Treatment is started with a small dose (Table 24 6) and gradually increased until benefit occurs or side effects limit further increments If treatment is ineffective, the drug is gradually withdrawn and another preparation then tried Common side effects include dryness of the mouth, nausea, constipation, palpitations, cardiac arrhythmias, urinary retention, confusion, agitation, restlessness, drowsiness, mydriasis, increased intraocular pressure, and defective accommodation Anticholinergic drugs are contraindicated in patients with prostatic hyperplasia, narrow-angle glaucoma, or obstructive
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Diagnostic problems may occur in mild cases, especially if tremor is minimal or absent For example, mild hypokinesia or slight tremor is commonly attributed to old age Depression, with its associated expressionless face, poorly modulated voice, and reduction in voluntary activity, can be difficult to distinguish from mild parkinsonism, especially since the two disorders may coexist; in some cases, a trial of antidepressant drug therapy is necessary The family history, the character of the tremor, and lack of other neurologic signs should distinguish essential tremor from parkinsonism Wilson s disease can be distinguished by its early age at onset, the presence of other abnormal movements, Kayser-Fleischer rings, and chronic hepatitis, and by increased concentrations of copper in the tissues Huntington s disease presenting with rigidity and bradykinesia may be mistaken for parkinsonism unless the family history and accompanying dementia are recognized In Shy-Drager syndrome (also called multisystem atrophy), the clinical features of parkinsonism are accompanied by autonomic insufficiency (leading to postural hypotension, anhidrosis, disturbances of sphincter control, impotence, etc) and more widespread neurologic deficits (pyramidal, lower motor neuron, or cerebellar signs) In progressive supranu-
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Table 24 6 Some anticholinergic antiparkinsonian drugs
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Drug Benztropine mesylate (Cogentin) Biperiden (Akineton) Orphenadrine (Disipal, Norflex) Procyclidine (Kemadrin) Trihexyphenidyl (Artane) Usual Daily Dose 1 6 mg 2 12 mg 150 400 mg 75 30 mg 6 20 mg
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Modified, with permission, from Aminoff MJ: Pharmacologic management of parkinsonism and other movement disorders In: Basic & Clinical Pharmacology, 10th ed Katzung BG (editor) McGraw-Hill, 2007
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gastrointestinal disease and are often tolerated poorly by the elderly 3 Levodopa Levodopa, which is converted in the body to dopamine, improves all of the major features of parkinsonism, including bradykinesia, but does not stop progression of the disorder The most common early side effects of levodopa are nausea, vomiting, and hypotension, but cardiac arrhythmias may also occur Dyskinesias, restlessness, confusion, and other behavioral changes tend to occur somewhat later and become more common with time Levodopainduced dyskinesias may take any conceivable form, including chorea, athetosis, dystonia, tremor, tics, and myoclonus An even later complication is the on-off phenomenon, in which abrupt but transient fluctuations in the severity of parkinsonism occur unpredictably but frequently during the day The off period of marked bradykinesia has been shown to relate in some instances to falling plasma levels of levodopa During the on phase, dyskinesias are often conspicuous but mobility is increased Carbidopa, which inhibits the enzyme responsible for the breakdown of levodopa to dopamine, does not cross the blood-brain barrier When levodopa is given in combination with carbidopa, the extracerebral breakdown of levodopa is diminished This reduces the amount of levodopa required daily for beneficial effects, and it lowers the incidence of nausea, vomiting, hypotension, and cardiac irregularities Such a combination does not prevent the development of the on-off phenomenon, and the incidence of other side effects (dyskinesias or psychiatric complications) may actually be increased Sinemet, a commercially available preparation that contains carbidopa and levodopa in a fixed ratio (1:10 or 1:4), is generally used Treatment is started with a small dose eg, one tablet of Sinemet 25/100 (containing 25 mg of carbidopa and 100 mg of levodopa) three times daily and gradually increased depending on the response Sinemet CR is a controlled-release formulation (containing 25 or 50 mg of carbidopa and 100 or 200 mg of levodopa) It is sometimes helpful in reducing fluctuations in clinical response to treatment and in reducing the frequency with which medication must be taken The commercially available combination of levodopa with both carbidopa and entacapone (Stalevo) may also be helpful in this context and is discussed in the following section on COMT inhibitors Response fluctuations are also reduced by keeping the daily intake of protein at the recommended minimum and taking the main protein meal as the last meal of the day The dyskinesias and behavioral side effects of levodopa are dose-related, but reduction in dose may eliminate any therapeutic benefit Levodopa-induced dyskinesias may also respond to amantadine Levodopa therapy is contraindicated in patients with psychotic illness or narrow-angle glaucoma It should not be given to patients taking monoamine oxidase A inhibitors or within 2 weeks of their withdrawal, because hypertensive crises may result Levodopa should be used with care in patients with suspected malignant melanomas or with active peptic ulcers because of concerns that it may exacerbate these disorders
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